Search for miracle cure goes on

Errors in some of the genes involved in obesity are probably common, but extreme problems of the sort experienced by this child are very rare. Genes are inherited in pairs, and because the correct one's version is preferred over the defective one, one good copy is enough to make you regulate weight normally.

Occasionally, both copies of a gene can be defective. The case is similar to two cases reported by Professor Steve O'Rahilly's Cambridge Institute for Medical Research. A child of eight - also of Bengali origin - was 86kg (190lb). Despite liposuction and surgery, she was no longer able to walk.

This genetic defect meant that her body was constantly telling her brain it was starving. People with this mutation will eat anything, to the extent that they will even eat flour or frozen fishfingers. The child has no control over this drive to eat, nor can the family control it.

The body has a "fat thermostat" that senses how much fat there is and adjusts eating or energy expenditure accordingly, to maintain a steady state or "set point" via a complex feedback system of chemicals - including a variety of hormones which control appetite and feeling full, as well as metabolic rate.

One of these hormones, leptin (from the Greek for thin) was discovered in 1995. It is made to a recipe supplied by the Ob gene, which was for a while hailed as the fat gene. Mice that had a defect in the Ob gene, and were grossly overweight, lost 30% of their body weight when given leptin and there was huge excitement that leptin would be the wonder obesity drug.

The bad news is that in humans, with the exception of those with a rare Ob mutation, the obese never seem to lose their ability to produce massive amounts of leptin and, although it may have a role for a tiny number of people, it is not going to be a miracle fat cure.

Some of us are born to binge because we have a fault in genes that convey the "I'm full" message to the brain. A study by Prof O'Rahilly found that of 500 people who became obese in early life, 6% had a mutation of this particular gene.